Journal of Biotechnology & Biomaterials
Open Access

Review Article

The Tripeptide, GHK, Induces Programmed Cell Death in SH-SY5Y Neuroblastoma Cells

¹UAB Global and Community Leadership Program, University of Alabama at Birmingham

²Department of Biology, University of Alabama at Birmingham

³Department of Clinical and Diagnostic Sciences and Biochemistry and Molecular Genetics, University of Alabama at Birmingham

Corresponding Author:

M. Tino Unlap, PhD
Department of Clinical and Diagnostic Sciences
SHPB 476, University of Alabama at Birmingham
Birmingham, AL 35294
Tel: 205-934-7382
E-mail: unlap@uab.edu

Received date: July 02, 2012; Accepted date: August 06, 2012; Published date: August 09, 2012

Citation: Matalka LE, Ford A, Unlap MT (2012) The Tripeptide, GHK, Induces Programmed Cell Death in SH-SY5Y Neuroblastoma Cells. J Biotechnol Biomater 2:144. doi:10.4172/2155-952X.1000144

Copyright: © 2012 Matalka LE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

GHK-Cu is a tripeptide that is found in plasma and increases fibroblast proliferation and is widely used in wound healing creams. Studies show that GHK-Cu stimulates the level of p63, a member of the antitumor suppressor family which includes p53 and p73. Because of its effect on p63, we tested the hypothesis that GHK induces apoptosis in neuroblastoma cells, SH-SY5Y, and that modification of GHK by polyethylene glycol (PEG) conjugation, PEGylation, potentiates its effects. Initial studies on NIH-3T3 fibroblasts and U937 histiocytic lymphoma cells show that GHK-Cu and GHK-PEG stimulate fibroblast proliferation while attenuating U937 cell proliferation. SH-SY5Y cells were treated with GHK or GHK-PEG at 1 and 10 nM for 24 hours followed by cell proliferation, cell viability, cell cytotoxicity and apoptosis assays. Our results showed that 24 hour GHK treatment elevated apoptosis by 1.8 ± 0.17 and 3.3 ± 0.15 fold at 1 and 10 nM, respectively. GHK-PEG treatment, on the other hand, stimulated apoptosis by 3.2 ± 0.80 and 4.9 ± 0.9 fold at 1 and 10 nM, respectively. The treatments, while having no effects on cell cytotoxicity, reduced neuroblastoma cell viability and cell proliferation. Therefore, GHK induces apoptosis in neuroblastoma cells, an affect which was potentiated by PEGylation.